Heart failure is a debilitating disease in which abnormal function of the heart leads in the direction of inadequate blood flow to fulfill the needs of the tissues and organs of the body. Typically, the heart loses propulsive power because the cardiac muscle loses capacity to stretch and contract. Often, the ventricles do not adequately eject or fill with blood between heartbeats and the valves regulating blood flow become leaky, allowing regurgitation or back-flow of blood. The impairment of arterial circulation deprives vital organs of oxygen and nutrients. Fatigue, weakness and the inability to carry out daily tasks may result. Not all heart failure patients suffer debilitating symptoms immediately. Some may live actively for years. Yet, with few exceptions, the disease is relentlessly progressive. As heart failure progresses, it tends to become increasingly difficult to manage. Even the compensatory responses it triggers in the body may themselves eventually complicate the clinical prognosis. For example, when the heart attempts to compensate for reduced cardiac output, it adds muscle causing the ventricles to grow in volume in an attempt to pump more blood with each heartbeat. This places a still higher demand on the heart's oxygen supply. If the oxygen supply falls short of the growing demand, as it often does, further injury to the heart may result. The additional muscle mass may also stiffen the heart walls to hamper rather than assist in providing cardiac output. A particularly severe form of heart failure is congestive heart failure (CHF) wherein the weak pumping of the heart leads to build-up of fluids in the lungs and other organs and tissues.
Heart failure has been classified by the New York Heart Association (NYHA) into four classes of progressively worsening symptoms and diminished exercise capacity. Class I corresponds to no limitation wherein ordinary physical activity does not cause undue fatigue, shortness of breath, or palpitation. Class II corresponds to slight limitation of physical activity wherein such patients are comfortable at rest, but wherein ordinary physical activity results in fatigue, shortness of breath, palpitations or angina. Class III corresponds to a marked limitation of physical activity wherein, although patients are comfortable at rest, even less than ordinary activity will lead to symptoms. Class IV corresponds to inability to carry on any physical activity without discomfort, wherein symptoms of heart failure are present even at rest and where increased discomfort is experienced with any physical activity.
The current standard treatment for heart failure is typically centered on medical treatment using angiotensin converting enzyme (ACE) inhibitors, diuretics, beta-blockade, and digitalis. Cardiac resynchronization therapy (CRT) may also be employed, if a bi-ventricular pacing device is implanted. Briefly, CRT seeks to normalize asynchronous cardiac electrical activation and resultant asynchronous contractions associated with CHF by delivering synchronized pacing stimulus to both ventricles. The stimulus is synchronized so as to improve overall cardiac function. This may have the additional beneficial effect of reducing the susceptibility to life-threatening tachyarrhythmias. CRT and related therapies are discussed in, for example, U.S. Pat. No. 6,643,546 to Mathis et al., entitled “Multi-Electrode Apparatus and Method for Treatment of Congestive Heart Failure”; U.S. Pat. No. 6,628,988 to Kramer et al., entitled “Apparatus and Method for Reversal of Myocardial Remodeling with Electrical Stimulation”; and U.S. Pat. No. 6,512,952 to Stahmann et al., entitled “Method and Apparatus for Maintaining Synchronized Pacing,” which are incorporated by reference herein.
In view of the potential severity of heart failure, it is highly desirable to detect its onset within a patient and to track its progression or regression so that appropriate therapy can be provided. Many patients suffering heart failure already have pacemakers or ICDs implanted therein or are candidates for such devices. Accordingly, it is desirable to provide such devices with the capability to automatically detect and track heart failure and, heretofore, a number of attempts have been made to provide for monitoring of physiological parameters associated with heart failure using implantable cardiac devices in conjunction with physiological sensors.
For example, U.S. Pat. No. 6,572,557, to Tchou et al., entitled “System and Method for Monitoring Progression of Cardiac Disease State Using Physiologic Sensors,” describes a technique for monitoring physiological parameters associated with the progression, stabilization, or regression of symptoms of heart disease such as CHF. The monitoring is implemented by ongoing surrogate measurement of standard and direct measurements, such as daily activity and respiratory and cardiac rate response, utilizing existing implantable, rate-responsive stimulation devices that incorporate activity, respiration, and/or other sensors. The system includes a sensor that measures activity and/or minute ventilation when triggered by changes in the sensed intrinsic heart rate and/or changes in a sensor-indicated pacing rate.
U.S. Pat. No. 6,645,153, to Kroll et al., entitled “System and Method for Evaluating Risk of Mortality Due to Congestive Heart Failure Using Physiologic Sensors,” describes a technique for determining a CHF mortality risk metric based on a combination of estimated ventilatory response values and the slope of heart rate reserve as a function of predicted heart rates. Ventilatory response is estimated based on detected values of actual heart rate, arterial oxygen saturation, right ventricular oxygen, stroke volume, tidal volume, and respiration rate. Heart rate reserve values are derived from the actual heart rate along with patient age and rest heart rate. The predicted heart rates, which represent the heart rates the patient would achieve if healthy, are derived from activity sensor signals. The CHF mortality risk metric is then calculated as a ratio of ventilatory response and the slope of the heart rate reserve.
U.S. Pat. No. 6,438,408 to Mulligan et al., entitled “Implantable Medical Device for Monitoring Congestive Heart Failure,” sets forth a technique for evaluating CHF that measures a group of parameters indicative of the state heart failure by employing electrocardiogram (EGM) signals, blood pressure (including absolute pressure, developed pressure, and change in pressure with time), and heart chamber volumes, specifically end systolic volumes (ESV). Based upon these signals, the technique operates to generate sets of parameters including (1) a relaxation or contraction time constant; (2) a mechanical restitution value; (3) a recirculation fraction value; and (4) an end systolic elastance value, indicative of the ratio of end systolic blood pressure to end systolic volume. Then, based upon a combination of these parameters, the system seeks to track changes in a heart failure with time.
A significant problem with many of the aforementioned techniques is their complexity. In many cases, multiple sensors are required for detecting multiple signals, which are then combined using fairly complex algorithms in an attempt to evaluate and track heart failure. It would be desirable to instead provide an effective but much more straightforward technique for evaluating heart failure, which does not require special sensors or complex algorithms. In addition, at least insofar as the techniques of Mulligan et al. are concerned, which operate to detect ESV (among many other parameters), it is believed that ESV and parameters derived therefrom are not as reliable an indicator of heart failure as would be preferred. In contrast, it has been recognized that left ventricular end-diastolic pressure (EDP), alone or in combination with other parameters, is a more effective parameter for use in tracking heart failure. However, there are technical challenges to the reliable detection of left ventricular EDP and so techniques exploiting left ventricular EDP have, heretofore, not been effectively implemented.
Accordingly, it would be desirable to provide alternative techniques for evaluating and tracking heart failure. In the technique of the parent application, also described herein below, ventricular end-diastolic volume (EDV) is used as a proxy for ventricular EDP. Briefly, values representative of EDV are detected using ventricular electrodes and then heart failure within the patient is evaluated based on ventricular EDV. In this manner, ventricular EDV is used as a proxy for ventricular EDP. By using ventricular EDV instead of ventricular EDP, heart failure is detected and evaluated without requiring sophisticated sensors or complex algorithms. Ventricular EDV is easily and reliably measured using impedance signals sensed by implanted ventricular pacing/sensing electrodes. The severity of heart failure is also evaluated based on ventricular EDV values and heart failure progression is tracked based on changes, if any, in ventricular EDV values over time.
Although the techniques of the parent application are very effective in detecting and tracking heart failure that has already occurred within a patient, it would also desirable to provide techniques for predicting the onset of heart failure or other heart conditions within patients. It is to that end that aspects of the present invention are directed. It would also be desirable to provide predictive techniques that distinguish between different types of heart failure, such as between diastolic heart failure (DHF) and systolic heart failure (SHF). It is to that end that others aspects of the present invention are directed.
Additionally, it is desirable to predict pulmonary edema that may arise due to heart failure. Pulmonary edema is a swelling and/or fluid accumulation in the lungs often caused by heart failure (i.e. the edema represents one of the “congestives” of CHF.) Briefly, the poor cardiac function resulting from heart failure can cause blood to back up in the lungs, thereby increasing blood pressure in the lungs. The increased pressure pushes fluid—but not blood cells—out of the blood vessels and into lung tissue and air sacs. This can cause severe respiratory problems and, left untreated, can be fatal. Pulmonary edema is usually associated with relatively severe forms of heart failure and is often asymptomatic until the edema itself becomes severe, i.e. the patient is unaware of the pulmonary edema until it has progressed to a near fatal state when respiration suddenly becomes quite difficult. Accordingly, it would be desirable to provide techniques for predicting the onset of pulmonary edema and still other aspects of the invention are directed to that end.